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PubMed1989

Ascorbic acid transport and accumulation in human neutrophils.

The transport, accumulation, and distribution of ascorbic acid were investigated in isolated human neutrophils utilizing a new ascorbic acid assay, which combined the techniques of high performance liquid chromatography and coulometric electrochemical detection. Freshly isolated human neutrophils contained 1.0-1.4 mM ascorbic acid, which was localized greater than or equal to 94% to the cytosol, was not protein bound, and was present only as ascorbic acid and not as dehydroascorbic acid. Upon addition of ascorbic acid to the extracellular medium in physiologic amounts, ascorbic acid was accumulated in neutrophils in millimolar concentrations. Accumulation was mediated by a high affinity and a low affinity transporter; both transporters were responsible for maintenance of concentration gradients as large as 50-fold. The high affinity transporter had an apparent Km of 2-5 microns by Lineweaver-Burk and Eadie-Hofstee analyses, and the low affinity transporter had an apparent Km of 6-7 mM by similar analyses. Each transporter was saturable and temperature dependent. In normal human blood the high affinity transporter should be saturated, whereas the low affinity transporter should be in its linear phase of uptake.

Ascorbic Acid↗
PubMed1984

Biochemical and functional-structural aspects of human cervical mucus.

Human cervical mucus is composed of an insoluble polymer of glycoproteins (mucin) which forms a matrix in which the aqueous phase is dispersed. Both the mucin and the aqueous phase are considered to be of importance to the structural integrity and function of cervical mucus. The mucin is considered to be composed of coiled glycoprotein molecules. These molecules may then associate by the chelation of divalent copper, via the carboxylic acid groups of the terminal sialic acid moieties of the carbohydrate side chains, to form the mucin per se. The modulation of the mucin structure at midcycle may then be achieved by the reduction of the copper bound to the sialic acid, by the oxidation of L-ascorbic acid: the L-ascorbic acid becoming oxidized to dehydroascorbic acid. This will result in an increase in hydration of the mucin by the association of water molecules with the uncomplexed sialic acid molecules of the glycoproteins. Thus the biophysical changes of cervical mucus may occur without enzymatically induced biochemical reactions. The proposed biochemical structure of cervical mucus is in accordance with the honeycomb-like structure of cervical mucin viewed by scanning electron microscopy. Whether or not the mucin exists precisely in this form in vivo is debatable. However, the honeycomb-like structure provides a convenient model on which one may investigate the biochemical, physiological and pathological nature of cervical mucus.

Ascorbic Acid↗
PubMed1983

Promoting effects of sodium L-ascorbate on two-stage urinary bladder carcinogenesis in rats.

The promoting effect of sodium L-ascorbate on two-stage urinary bladder carcinogenesis in F344 rats initiated with N-butyl-N-(4-hydroxybutyl)nitrosamine at levels of 0.01 and 0.05% in drinking water was studied. Administration of 5.0% but not of 1.0% sodium L-ascorbate in the diet significantly increased the incidence and number of preneoplastic lesions, papillary or nodular hyperplasia, papilloma, and cancer of the urinary bladder. In groups given 5.0% sodium L-ascorbate, the urine was characterized by an apparent elevation of pH, a decrease of osmolality, and an increase of MgNH4PO4 crystalline. Addition of sodium L-ascorbate to the diet also resulted in increase in the content of ascorbic acid and its metabolite, dehydroascorbic acid, in the urine. These results show that an extremely high dose of sodium L-ascorbate (5.0%) promotes urinary bladder carcinogenesis under the present experimental conditions, while a high dose (1.0%) does not.

Animals↗
PubMed1991

Effect of combined ascorbic acid and B-12 on survival of mice with implanted Ehrlich carcinoma and L1210 leukemia.

A combination of dehydroascorbic acid and hydroxycobalamin (vitamin B-12) inhibited mitoses of tumors in mice. The present study was performed to test the effect of these vitamins on the survival of mice bearing carcinomas and leukemias. In each assay 40 mice received 0.1 mL ip tumor cells (x10(5)). After 24 h, 20 mice were injected with 0.2 mL (0.4 g/kg body wt) of the vitamins daily for 10 d. All controls died by day 19, but greater than 50% of the treated mice were alive after 60 d. In vitro findings revealed inhibition of mitoses in L1210 leukemia cells, but not in normal L929 cells. In recent research with cobalt-ascorbate plus vitamin C, we demonstrated that when B-12 is combined with vitamin C, the cobalt nucleus of B-12 attaches to a carbon on vitamin C, forming cobalt ascorbate. Tests proved that cobalt ascorbate plus vitamin C also inhibited tumor cells.

Animals↗
PubMed1995

The in vivo cytoprotection of ascorbic acid against ischemia/reoxygenation injury of rat liver.

The in vivo effects of ascorbic acid on the reoxygenated liver tissue were examined, with regard to the following effects: (i) the effects of scavenging radicals and/or reducing peroxidative reactions, and (ii) the effects of the chelation with low-molecular-weight iron and increasing its reactivity (radical production). Ascorbic acid is one of the water-soluble vitamins known to have various physiological effects involving both chelating and reducing properties at once. Lipid peroxidation of the reoxygenated liver tissue estimated by the production of TBARS (thiobarbituric acid-reactive substance) and LPO (lipid hydroperoxides) was suppressed effectively by the preischemic intraperitoneal administration of ascorbic acid. Ascorbic acid also showed this anti-oxidant effect in a dose-dependent manner. The analysis of the levels of ascorbic acid and glutathione of the liver tissue revealed that ascorbic acid works as an anti-oxidant probably by being oxydized finally to dehydroascorbic acid just after the reoxygenation. The latter was reduced to ascorbic acid again, coupled with the conversion of GSH to GSSG in the postischemic time course. The predominant effect of ascorbic acid on the reoxygenated liver tissue seems to be caused by the scavenging radicals and/or reducing peroxidative reactions, rather than by chelating iron and increasing its reactivity (radical production). Cellular integrity (estimated by the release of GOT, GPT, and LDH) and the energy state of the postischemic liver tissue (estimated by the tissue ATP level) were also well preserved by the administration of ascorbic acid.

Adenosine Triphosphate↗
PubMed2003

Biochemical changes in arthritic rats: dehydroascorbic and ascorbic acid levels.

The objective of this work was to evaluate the use of vitamin C as a biomarker in the inflammatory phase of the rat adjuvant arthritis and to correlate it with other parameters used for disease evaluation. Paw swelling was used for physical evaluation and the levels of ascorbate and dehydroascorbate in the serum of male rats, before and after adjuvant arthritis induction, were quantified by a high-performance liquid chromatography method (HPLC). The optimised HPLC assay enabled the quantification of both forms of the vitamin in rat sera, with the same extraction method and using different detectors, instead of obtaining dehydroascorbate by subtraction of the total ascorbate measurement. This method was used to follow the severity of adjuvant arthritis and the results were correlated with other already established disease activity parameters. A decrease of ascorbic acid and dehydroascorbic acid was observed with the increase of right paw circumference during the course of adjuvant arthritis. The disease associated changes in the serum concentrations of ascorbic acid, from biosynthesis and from recycling, can be evaluated by the direct quantification of dehydroascorbic acid. This provides some evidence for the potential of the quantification of these biomarkers to study the disease activity, and as a tool for the establishment of therapeutic protocols, to evaluate the anti-inflammatory effect of new drugs or formulations.

Animals↗
PubMed1975

Effects of reducing and oxidizing agents on the action of bleomycin.

The effects of reducing agents, such as 2-mercaptoethanol, dithiothreitol, L-ascorbic acid, or sodium borohydride, and oxidizing agents, such as hydrogen peroxide or dehydroascorbic acid, on the in vitro action of bleomycin were investigated. After the incubation of DNA with a low concentration of bleomycin and a reducing or oxidizing agent, single strand breaks were mainly caused in the DNA molecules. The degradation of DNA was largely prevented by the removal of oxygen, or by the addition of divalent cations or of S-(2-aminoethyl)isothiuronium bromide hydrobromide, a radical scavenger, to the incubation mixture. Preincubation of bleomycin with these reducing or oxidizing agents reduced the DNA-degrading activity of the antibiotic. However, this reduction in activity was observed even in the absence of oxygen, or in preincubation mixture supplemented with radical scavenger.

Ascorbic Acid↗
PubMed1981

Ascorbic acid metabolism in diabetes mellitus.

In contrast to normal subjects diabetic patients and very low plasma ascorbic acid and significantly high (p less than 0.001) dehydroascorbic acid irrespective of age, sex, duration of the disease, type of treatment, and glycemic control. However, there was no significant difference between the mean leukocyte ascorbate concentrations of the two populations. The in vitro rates of dehydroascorbate reduction in the hemolysate and the erythrocyte reduced glutathione levels and the glucose-6-phosphate dehydrogenase activities, which regulate the dehydroascorbate reduction, were similar in normal and diabetic subjects. The turnover of ascorbic acid was higher in the diabetics than that in the normal volunteers. Experiments with diabetic rats indicated that the increased turnover of ascorbic acid was probably due to increased oxidation of ascorbate to dehydroascorbate in tissue mitochondria. Ascorbic acid supplementation at a dose of 500 mg per day for a brief period of 15 days resulted in an increase in the plasma ascorbate level temporarily, but it did not lower the blood glucose level of the diabetic patients.

Adolescent↗
PubMed1991

The effect of cyanide on vitamin C uptake by human polymorphonuclear leukocytes.

1. Cyanide inhibited the uptake of vitamin C by human polymorphonuclear leukocytes (PMNs). 2. Preincubation of PMNs with cyanide had no effect on cytochalasin B-inhibitable uptake of dehydroascorbic acid (DHA) (the reversibly oxidized and transportable form of vitamin C). 3. Preincubation of DHA with cyanide resulted in inhibition of DHA uptake. 4. Vitamin C uptake was decreased by cyanide to the same degree as it was by glutathione (GSH), which effectively reduces DHA to ascorbic acid. The effects of cyanide and GSH were not additive. 5. The data are consistent with the hypothesis that cyanide inhibition of vitamin C uptake represents the chemical elimination of extracellular DHA rather than the inhibition of active transport in these cells.

Animals↗
PubMed1993

Monodehydroascorbate reductase activity in the surface membrane of leukemic cells. Characterization by a ferricyanide-driven redox cycle.

A transmembrane monodehydroascorbate reductase activity with a high affinity in the subpicomolar concentration range of the free radical can be measured at the surface of erythroleukemic cells using a ferricyanide-driven redox cycle. The activity is dependent on the membrane potential and can therefore only be found in intact cells. It is independent of the glutathione content of the cells. Thenoyltrifluoroacetone is an efficient inhibitor of the activity, whereas ouabain, monensin and tetraethylammonium show no effect. Cells are able to generate ascorbate from dehydroascorbic acid. This explains why both forms of vitamin C show practically the same affinity for the redox cycle but why it does not drive the redox cycle by itself because it is much slower and is not inhibited by thenoyltrifluoroacetone. The reductase activity is independent of the degree of differentiation of the leukemic cells.

Animals↗
PubMed1978

Cell survival in V79 multicell spheroids treated with dehydroascorbate, 5-thio-D-glucose and 2-deoxy-D-glucose.

We found that dehydroascorbic acid (DHA), 5-thio-D-glucose (5TG) and 2-deoxy-D-glucose (2DG) were toxic to monolayers of V79 cells under hypoxic conditions at 37 degree C but not at 0 degree C. Very little toxicity was observed at either temperature under aerobic conditions. When spheroids (600 micrometer diameter) were treated with 7.5 mM of these chemicals for periods up to 3 days, the number of viable cells per spheroid dropped to 70% for DHA, 50% for 5TG and 25% for 2DG relative to controls. These survivals were reduced to much lower values when the experiments were repeated in glucose-free medium.

Ascorbic Acid↗
PubMed1979

Effect of flavonoids on vitamin C activity of D-isoascorbic acid.

Large peroral doses of D-isoascorbic acid, a vitamin C stereoisomer (50 mg per animal per day), were retained in the guinea-pig organism to a smaller extent than the same doses of L-ascorbic acid (vitamin C). Simultaneous administration of the flavonoids rutin and epicatechin increased the amount of D-isoascorbic acid retained in the liver, brain and wall of the small intestine by up to 100%, but four weeks after its extraction from the food the amount of L-ascorbic acid left in the guinea-pig organism still exceeded D-isoascorbic acid reserves. This difference, which was found in all the organs studied, was the largest in the groups simultaneously given flavonoids. In guinea-pigs which, like man, are dependent on an exogenous vitamin C supply, D-isoascorbic acid was metabolized at a manifestly higher rate than L-ascorbic acid, irrespective of whether flavonoids were administered or not. In liver, brain and small intestine wall homogenates, the oxidized forms of both stereoisomers were reduced in the presence of reduced glutathione, but the reduction rate of D-isodehydroascorbic acid was higher and it was stimulated by the two flavonoids more strongly than the reduction of L-dehydroascorbic acid. The stuterospecific.

Adrenal Glands↗
PubMed1976

Stability of vitamin C (ascorbic acid) in tablets.

Stability of ascorbic acid (vitamin C) in various tablet formulations and the nature and extent of formation of decomposition products (dehydroascorbic acid, diketogulonic acid, and oxalic acid) were determined under normal conditions of storage and in simulated use tests. IR spectrophotometric, colorimetric, fluorometric, titrimetric, polarographic, and chromatographic methods were applied. Recent implications concerning the instability of ascorbic acid in tablets and the potentially harmful nature of the breakdown products are shown to be unfounded. Under normal storage conditions, commerical-type ascorbic acid tablets are stable for over 5 years (greater than 95% potency retention). The amounts of all three breakdown products formed under the various storage conditions constitute a small percentage of the ascorbic acid content and pose no dietary hazard. IR spectroscopy was inadequate as a quantitative method for evaluating ascorbic acid potency in tablet formulations. The official titration methods and TLC, colorimetric, and polarographic determinations correlate well and define accurately the stability of ascorbic acid in these dosage forms.

Ascorbic Acid↗
PubMed1979

Absorption of vitamin C from the human buccal cavity.

1. Ascorbic acid was absorbed across the mucosa of the human mouth. 2. Omission of sodium ions from the medium decreased the absorption of ascorbic acid. 3. The presence of D-glucose, or 3-O-methyl-D-glucose, increased the absorption of ascorbic acid but D-fructose had little effect and D-mannitol had no effect. 4. Calcium ions also increased ascorbic acid absorption probably by a secondary effect on "Na+ fluxes. 5. Buccal mucosa was also permeable to dehydroascorbic acid and D-isoascorbic acid.

Absorption↗
PubMed1994

Transport of vitamin C in animal and human cells.

The transport systems of animal and human tissues for vitamin C are reviewed with respect to their properties. It emerges that pure diffusion plays only a very minor role while a variety of more or less specific transporters is found on cellular membranes. Although most tissues prefer the reduced ascorbate over the oxidized dehydroascorbic acid and have high-affinity transporters for it, there are several examples for the reversed situation. Special attention is given to similarity or identity with glucose transporters, especially the GLUT-1 and the sodium-dependent intestinal and renal transporters, and to the very widespread dependence of ascorbate transport on sodium ions. The significance of ascorbate transport for vitamin C-requiring and nonrequiring species as well as alterations in states of disease can be seen from ample experimental evidence.

Animals↗
PubMed1996

Validation of a micromethod for determining oxidized and reduced vitamin C in plasma by HPLC-fluorescence.

An HPLC micro-method with fluorescence detection has been developed to determine total vitamin C (vit C) and dehydroascorbic acid (DHA) concentrations in human plasma samples. This method is based on the rapid, specific reaction of DHA with dimethyl-o-phenylenediamine (DMPD) to form a fluorescent quinoxaline derivative that is quantified by HPLC in less than 5 minutes. The method was assessed with reference to the direct 2,4-dinitrophenylhydrazine (DNPH) colorimetric method. They were well correlated (r3 = 0.879), but the DMPD-HPLC method had the limit of detection 6 times lower than the standard method and the relative error for a vitamin standard was 10 times better than that of the standard method. The plasma DHA to total vit C ratio varied from 10 to 60%, depending on sample processing. Plasma that were immediately analysed contained 10% DHA whatever the subject's age; frozen deproteinized samples kept 1 week (-67 degrees C) had 20%, and blood samples kept for one hour at room temperature before treatment had up to 60% DHA. The ratio in capillary samples taken from the finger was 11-42%. This rapid, specific and very sensitive micro-method is well suited to routine measurements of plasma vit C.

Adult↗
PubMed2005

Role of endogenous melatonin in the oxidative homeostasis of the extracellular striatal compartment: a microdialysis study in PC12 cells in vitro and in the striatum of freely moving rats.

A capillary apparatus for in vitro microdialysis was used to investigate melatonin and ascorbic acid effects on dopamine (DA) autoxidation or nitric oxide (NO)-mediated oxidation in suspended PC12 cells. Following high K+ (KCl 75 mm) infusion, secreted DA underwent a partial autoxidation or peroxynitrite-mediated oxidation when the potential peroxynitrite generator 3-morpholinosydnonimine (SIN-1, 1.0 mm) was co-infused with KCl. Ascorbic acid was supplied to the medium by means of intracellular reduction of infused dehydroascorbic acid (DHAA) (5.0 mm). Melatonin (50 microm) and DHAA showed a synergistic effect in inhibiting DA autoxidation and peroxynitrite-mediated DA oxidation. Moreover, melatonin increased dialysate recovery of ascorbic acid released from PC12 cells. Endogenous melatonin was depleted in rats maintained on a 24-hr light cycle for 1 wk. In melatonin-depleted rats, baseline levels of dialysate ascorbic acid were lower than controls, while those of DA were unaffected. In these rats, intrastriatal infusion of 5.0 mm SIN-1 induced DA increases significantly lower than in controls; in addition, dialysate ascorbic acid concentrations exhibited significant decreases. Melatonin co-infusion restored SIN-1 effects on dialysate DA and antagonized SIN-1-induced ascorbic acid decreases. Melatonin-depleted rats were allowed to recover. In these rats, striatal baseline ascorbic acid, as well as SIN-1-induced increases in dialysate DA did not differ from controls. Taken together, these findings suggest that endogenous melatonin is an active component of the striatal extracellular antioxidant pool, as it maintains endogenous ascorbic acid in its reduced status and co-operates with ascorbic acid in protecting extracellular DA from exogenous NO-mediated oxidation.

Animals↗
PubMed2004

Enhancing effects of intracellular ascorbic acid on peroxynitrite-induced U937 cell death are mediated by mitochondrial events resulting in enhanced sensitivity to peroxynitrite-dependent inhibition of complex III and formation of hydrogen peroxide.

A short-term pre-exposure to dehydroascorbic acid (DHA) promotes U937 cell death upon exposure to otherwise non-toxic levels of peroxynitrite (ONOO-). Toxicity is mediated by a saturable mechanism and cell death takes place as a consequence of mitochondrial permeability transition. The following lines of evidence are consistent with the notion that the enhancing effects of DHA were related to mitochondrial events resulting in inhibition of complex III upon exposure to otherwise inactive concentrations of ONOO-. First, DHA, as well as bona fide complex III inhibitors, similarly enhanced toxicity and subsequent formation of H2O2 induced by ONOO- via a rotenone- or catalase-sensitive mechanism. Secondly, bona fide complex III inhibitors were ineffective in DHA-pre-loaded cells. In addition, respiration-deficient cells were resistant to toxicity elicited by ONOO- and their supplementation with increasing concentrations of DHA, although resulting in the accumulation of vitamin C levels identical with those observed in respiration-proficient cells, failed to affect ONOO- toxicity. Finally, oxygen-consumption experiments demonstrated that pre-exposure to DHA promotes the ONOO--dependent inhibition of complex III. In conclusion, the above results collectively demonstrate that increasing the intracellular accumulation of vitamin C promotes mitochondrial events leading to ONOO--dependent formation of H2O2 and resulting in a rapid necrotic response.

Ascorbic Acid↗